Bacteriology & Parasitology

advertisement
Bacteriology & Parasitology
Samuel, J Bacteriol Parasitol 2016, 7:1
http://dx.doi.org/10.4172/2155-9597.1000261
Review Article
Open Access
Opportunistic Parasitism: Parasitic Association with the Host that has
Compromised Immune System
Fikresilasie Samuel
Department of Medicine, Ambo University, Ambo, Ethiopia
*Corresponding
author: Fikresilasie Samuel, Department of Medicine, Ambo University, Ambo, Ethiopia, Tel: +251929050512; E-mail: fikre16sam@gmail.com
Received date: October 05, 2015; Accepted date: February 17, 2016; Published date: February 23, 2016
Copyright: © 2016 Samuel F. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use,
distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
A symbiotic association between opportunistic parasites and immunocompromised hosts is known as
opportunistic parasitism. The abnormality of immunity is caused by different factors: Aging enhances susceptibility to
severe infections; malnutrition has significant depressing consequences for immune function; an
immunosuppressant substance alcohol can interfere with the functions of many of the cells and molecules those are
components of the immune system; infectious pathogens are also major causal agents of immunosuppression.
Combined effect of these factors makes the host to be susceptible for opportunistic parasitic infections. In this review
the promising factors which induce immune disorder and exemplary opportunistic parasitic infections which illustrate
the real sense of opportunistic parasitism are well discussed.
Keywords: Opportunistic parasite; Immunity; Host; Parasitism
Introduction
Opportunistic parasitism can be defined as a symbiotic association
between opportunistic parasites and immunocompromised hosts; so
that the parasite causes opportunistic parasitic infection (OPI). OPI
occur enthusiastically with organisms that are recognized pathogens,
but are commonly caused by commensals or other normally nonpathogenic agents when host resistances are weaken by different
environmental or natural factors [1].
OPI may not cause severe pathological changes in
immunocompetent hosts as long as the immune system is functioning
normally [2]. However when the immune system is weaken due to
particular conditions, opportunistic parasites take this advantage to
initiate an infection [3]. Many people have impaired immune systems
as a result of many factors: diseases (like HIV infection or malignant
diseases), medical procedures (such as organ transplants) [2], aging,
chemotherapy and others. For these reasons, the system acquired
different defects (humeral or cell mediated). This will establish
favorable condition for opportunistic parasites to flourish over the host
system and cause a disease [4].
Review
The normal immune system task is depending on the interaction of
enormous variety of cells and molecules. Which may involves many
different mechanisms some nonspecific (i.e., generically applicable to
many different pathogenic organisms) and others specific (i.e., their
protective effect is directed to one single organism) to protect our body
from infectious agents. Nevertheless, multiplicity of different defects as
a result of diverse factors can diminish its competence badly; these
deficiencies put in the same end- result, increased susceptibility to
infection [5,6]. This review discusses the basic concept of opportunistic
parasitism and provides better definition of this association via
explaining major factors which induce immune system impairment. As
J Bacteriol Parasitol
ISSN:2155-9597 JBP, an open access journal
well, three opportunistic parasitic infections are well discussed to
exemplify others.
Major Risk Factors and Immune System Impairment
Age and stress
Resistance to the disease tends to be weaker in childhood and old
age [7]. Aging enhances susceptibility to severe infections, which is
related with a depression of cellular immunity. It has direct
consequence on development of frequent and rigorous infection,
which further increases morbidity, dependence and fatality in elderly
population [8]. In addition to aging, the immuno-suppressive effect of
stress contributes to the immune defects that give rise to the prevalence
of infectious illnesses in older adults [9]. Studies on stress in older
adults provide evidence that increased stress exposure, poor stress
buffering, exaggerated stress reactivity, unlimited anxiety duration, and
probably diminished restorative processes have effects that mimic,
aggravate, and sometimes speed up the effects of aging on immunity
[9].
Malnutrition
Nutrition has been clearly identified as key factor for human
development, not only as a conditioning factor for health but also as
determinant of quality of life throughout the lifecycle and of overall
development. Specially, in order to function competently our immune
system needs nourishment [10]. Calorie, protein, vitamins and
minerals (such as iron, copper and zinc) intakes are very important [7].
The word ‘malnutrition’ expresses any disorder resulting from an
insufficient or unbalanced diets, or a malfunctioning to absorb or
assimilate nutritional elements. It could be protein-energy
malnutrition or micronutrient deficiencies [10]. Usually, poor protein
intake and insufficient amount of vitamins and minerals in the diet
have significant depressing consequences for immune function [11].
All these conditions are associated with significant impairments of
Volume 7 • Issue 1 • 1000261
Citation:
Samuel F (2016) Opportunistic Parasitism: Parasitic Association with the Host that has Compromised Immune System. J Bacteriol
Parasitol 7: 261. doi:10.4172/2155-9597.1000261
Page 2 of 4
cell-mediated immunity, antibody concentrations, phagocyte function,
complement system, and cytokine production [10,12].
Cryptosporidium spp are well recognized as causes of diarrheal disease
during waterborne epidemics and in immunocompromised hosts [18].
In conclusion, there is cyclical relationship between malnutrition
and immunity. Poor nourishment consequences weight loss, growth
faltering, lowered immunity and mucosal damage. These increase
vulnerability of the host to communicable diseases and lead to
immunological impairments. As a result, metabolic responses change
nutritional status of the individual through loss of appetite,
malabsorption and altered metabolism [13].
The degree of the disease is mostly dependent on the immune status
of the host, whether the infection is self-limiting or continual. It is well
known that, both branches of the immune system are required for
complete improvement of the disease [19]. The studies on the
mechanisms of immunity to cryptosporidiosis pointed out that, the
spectrum and severity of disease in immunocompromised individuals
with cryptosporidiosis reflect the importance of the T-cell response
since the most severe disease is seen in individuals with defects in the
T-cell response [20].
Alcohol
Alcohol is an immunosuppressant substance, which affects both cell
mediated and humeral immunity, as does severe malnutrition [14]. It
interferes with the functions of many of the cells and molecules those
are components of the immune system. For example, alcohol slows
down the functions of Phagocytes (i.e., neutrophils, Monocytes, and
macrophages). It also changes the production of signaling molecules
that facilitate to organize the immune response (i.e., cytokines) [15].
The dysfunction of the immune system makes the patient susceptible
to enormous collection of infectious pathogens, resulting in biomedical
consequences such as increased risk of infections after surgery,
traumatic injury, or burns; of liver disease; of opportunistic infections
in the lungs; and of accelerated development of HIV disease [14,16].
As a result, immunocompromised adults and children, especially
those with AIDS, children in day care, travelers to endemic regions,
dairy or cattle farm workers of their families or contacts, household
contacts of cases or carriers, and possibly owners of infected dogs or
cats or their neighbors are at greatest risk [21]. As well, individuals
with neoplasm, severe combined immunodeficiency syndrome and
acute leukemia (most commonly in children) are associated with
increased risk of severe cryptosporidiosis disease [20]. To conclude,
immunodeficiency increased the risk of having opportunistic parasites
and diarrhea. In the immunocompromised host, infection is
prolonged, sometimes asymptomatic, but may result in chronic
debilitating diarrhea with dehydration, malabsorption, and wasting
[22].
Infection and drug
Public health measures to reduce contamination of water supplies
and vigilant surveillance will reduce the risk to populations [23].
Besides, the widespread use of antiretroviral therapy does appear to be
having a beneficial effect on recovery from cryptosporidiosis and on
the frequency of infection in human immunodeficiency virus-positive
patients. Therefore, increasing patient immune status and screening at
least for those treatable parasites is important [24].
Infectious
pathogens
are
major
causal
agents
of
immunosuppression. Specially, acquired immunosuppression due to
pathogens is primarily caused by viruses that invade the cellular
compartment of the immune system [7]. For illustration, viral
infection of cells naturally leads to the secretion of interferon alpha
(IFNα) by that cell. It is protective for cells in the local setting. On the
contrary, IFNα inhibits the G1 phase of the cell cycle, producing a
momentary immunosuppression since cells responding to IFNα
cannot clonally enlarge. In addition to immunosuppression induced by
IFNα, the HIV itself induces immunosuppression in a number of ways,
the destruction of CD4+ T cells, cells necessary for almost every part of
immunity. Other viruses, such as measles, can too temporarily depress
T cell function [7].
Besides to infections, drugs recommended for treatment contribute
to impair the immune system. These cause immunodeficiency, either
purposely or accidentally [7]. For example, cancerous diseases are
often treated by administration of cytotoxic drugs intended to kill the
tumor cells. These drugs are not cancer cell-specific and other
proliferating cells are also destroyed. Cytotoxicity to immune cells
causes nonspecific immunosuppression. In addition, to combat the risk
of graft rejection, transplant patients are intentionally given
immunosuppressive drugs, many of which inhibit the secretion of
cytokines that enhance immune responses. These patients are thus at
risk of the same infectious disorders seen in other immune defects [5].
Exemplary Opportunistic Parasitic Infections
Cryptosporidiosis
Species of the genus Cryptosporidium are protozoan parasites
(Apicomplexa) that cause gastroenteritis in animals and humans. Of
these Cryptosporidium parvum and Cryptosporidium hominis are the
major causative agents of human cryptosporidiosis [17].
J Bacteriol Parasitol
ISSN:2155-9597 JBP, an open access journal
Toxoplasmosis
Toxoplasmosis is an opportunistic parasitic infection caused by
obligate intracellular protozoan parasite Toxoplasma gondii, a parasite
belonging to the phylum Apicomplexa. The disease is primarily
transmitted by ingesting undercooked or raw meat containing tissue
cysts, or by ingesting food or water contaminated with oocysts [6].
Toxoplasma invades any cell by an active invasion process involving
motility and molecular secretion. Its success as an invasive organism
resides on its high trans-epithelial migration capability reaching
privileged organs such as brain, eye and placenta in pregnant women.
Infection in pregnant women may lead to abortion, stillbirth or other
serious consequences in newborns [25]. Toxoplasmosis affects up to
one-third of the global human population. Sero-prevalence studies in
different communities of Ethiopia showed that the general prevalence
of the disease is about 80% in the adult population [6]. And up to 41%
in children aged 1-5 years [26].
Immunosuppression due to treatment after transplantation or
related with HIV infection raises exposure to numerous opportunistic
infections, counting toxoplasmosis. The disease central nervous system
(CNS) toxoplasmosis affects the brain and occurs almost exclusively
due to reactivation of latent infection [27]. It is very important
opportunistic infection in AIDS patients. Abnormal cytokine profile
and impaired cytotoxic T cell functionality are responsible for easy
susceptibility to this infection [28]. The lung is also a major site of
infection after the CNS toxoplasmosis in immunocompromised
peoples. AIDS patients having CD4+ T cell count <100 cells/μl of blood
Volume 7 • Issue 1 • 1000261
Citation:
Samuel F (2016) Opportunistic Parasitism: Parasitic Association with the Host that has Compromised Immune System. J Bacteriol
Parasitol 7: 261. doi:10.4172/2155-9597.1000261
Page 3 of 4
can have reactivation from asymptomatic latent infection. However,
most vulnerable patients are those having CD4+ T cell count <50 cells/
μl of blood [28].
In transplant recipients toxoplasmosis is common and clearly stated
in different studies. It occurs by reactivation of latent infection or is a
primary infection if a donor organ containing encysted T. gondii was
transplanted into a seronegative recipient [29]. In addition, studies in
Korea have announced that toxoplasmosis is a rare but can be fatal
complication in hematopoietic stem cell transplant recipients, usually
associated with allogeneic hematopoietic stem cell transplantation
(HSCT) [30].
Educating the public about the risks associated with unhealthy food
and life style habits, tracking serological examinations to special
populations and measures to strengthen food and occupational safety
are recommended to avoid toxoplasmosis [25]. Finally, ART treatment
lowers the incidence of toxoplasmosis in HIV patients [28].
factors which provoke the human immune system to be impaired. Such
as: age, infection, alcohol etc. So that opportunistic organisms use the
advantage to initiate an infection.
References
1.
2.
3.
4.
5.
Strongyloidiasis
6.
Strongyloidiasis is an infection caused by an intestinal nematode,
Strongyloides stercoralis, which has a cosmopolitan distribution in
tropical and subtropical regions. Infection is via trans-cutaneous by
filariform larvae. This usually leads to cutaneous, gastrointestinal, or
pulmonary symptoms depending on the host immune status [31]. It is
endemic world-wide, yet more prevalent in hot and humid climates as
well as resource poor countries with inadequate sanitary conditions
[32].
7.
S. stercoralis is unique among intestinal nematodes in its ability to
complete its life cycle within the host through an asexual auto-infective
cycle, allowing the infection to persist in the host indefinitely. Under
some conditions associated with immunocompromised, this
autoinfective cycle can become amplified into a potentially fatal
hyperinfection syndrome, characterized by gastrointestinal bleeding
and respiratory distress [33]. It makes S. stercoralis opportunistic
parasite, which occurs frequently in immunocompromised patients,
especially in those with a defect in cell-mediated immunity [34].
A variety of underlying conditions appear to predispose to severe
infections. Including immunodeficiency due to defective T-lymphocyte
function, therapeutic regimens consisting of corticosteroids or other
immunosuppressive medication, and chronic illness or malnutrition,
predispose to systemic strongyloidiasis. Studies suggested that this
infection incorporate unexplained gram-negative bacillary bacteremia
in a compromised host [32].
Measurement like screening for Strongyloides infection before the
initiation of immunosuppressive therapy should be considered in
patients with unexplained eosinophilia, serpiginous skin lesions, or
pulmonary or gastrointestinal symptoms [31,35]. Furthermore,
transplantation centers drawing patients from areas with endemic
Strongyloides should evaluate potential recipients closely for occult
strongyloides infection prior to initiating immunosuppressive therapy
[34]. To conclude, after immunocompromised patients develop
hyperinfection syndrome, diagnosis is often delayed and mortality is
high, as a result emphasis should be placed on testing and treatment
prior to transplantation
Conclusion
OPIs are well flourished in immunocompromised individuals,
whose immune system has defects to function normally. There are
J Bacteriol Parasitol
ISSN:2155-9597 JBP, an open access journal
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
Peter JD, Ivan MR (1998) Encyclopedia of immunology (2nd edn).
Volume 1.
Zope A, Pai A, De A, Baveja SM (2014) Opportunistic Intestinal Parasites
in HIV Infected Individuals and Its Correlation with the Cd4 Counts.
Research and Reviews: Journal of Medical and Health Sciences.
Kashyap A, Singh MP, Ghoshal U (2013) Occurrence of Gastrointestinal
Opportunistic Parasites in Immunocompromised Patients in Northern
India. Journal of Biology 1: 77-80.
FMOH (2008) Guidelines for management of opportunistic infections
and Anti-Retroviral Treatment in adolescents and adults in Ethiopia.
Addis Ababa, Ethiopia.
Gorczynski R, Stanley J (1999) Clinical immunology. Landes Bioscience,
Texas.
Eales LJ (2003) Immunology for Life Scientists. John Wiley & Sons Ltd,
England.
Playfair JHL, Chain BM (2001) Immunology at a glance. Blackwell
Publishing, USA.
Dey AB, Chatterjee P, Das PC (2012) Immune Status in the Elderly.
Medicine Update.
Hawkley LC, Cacioppo JT (2004) Stress and the aging immune system.
Brain Behav Immun 18: 114-119.
Duggal S, Chugh TD, Duggal AK (2012) HIV and malnutrition: effects on
immune system. Clin Dev Immunol 2012: 784740.
Sicotte M, Langlois EV, Aho J, Ziegle D, Zunzunegui, MV (2014)
Association between nutritional status and the immune response in HIV
+ patients under HAART: protocol for a systematic review. Systematic
Reviews 3: 9.
Huhhes S, Kelly P (2006) Interaction of malnutrition and immune
impairment, with specific reference to immunity against parasites.
Parasite immunology 28: 577-588.
Keusch GT (2003) The history of nutrition: malnutrition, infection and
immunity. J Nutr 133: 336S-340S.
Molina PE, Happel KI, Zhang P, Kolls JK, Nelson S (2010) Focus on:
Alcohol and the immune system. Alcohol Res Health 33: 97-108.
Szabo G (1997) Alcohol's contribution to compromised immunity.
Alcohol Health Res World 21: 30-41.
Greenfield TK, Ye Y, Bond J, Kerr WC, Nayak MB, et al. (2014) Risks of
alcohol use disorders related to drinking patterns in the U.S. general
population. J Stud Alcohol Drugs 75: 319-327.
Rossle NF, Latif B (2013) Cryptosporidiosis as threatening health
problem: A review. Asian Pac J Trop Biomed 3: 916-924.
Checkley W, White AC Jr, Jaganath D, Arrowood MJ, Chalmers RM, et al.
(2015) A review of the global burden, novel diagnostics, therapeutics, and
vaccine targets for cryptosporidium. Lancet Infect Dis 15: 85-94.
McNair NN, Mead JR (2013) CD4⁺ effector and memory cell populations
protect against Cryptosporidium parvum infection. Microbes Infect 15:
599-606.
Hunter PR, Nichols G (2002) Epidemiology and clinical features of
Cryptosporidium infection in immunocompromised patients. Clin
Microbiol Rev 15: 145-154.
Desai NT, Sarkar R, Kang G (2012) Cryptosporidiosis: An underrecognized public health problem. Trop Parasitol 2: 91-98.
Mead JR (2014) Prospects for immunotherapy and vaccines against
Cryptosporidium. Hum Vaccin Immunother 10: 1505-1513.
Peletz R, Mahin T, Elliott M, Montgomery M, Clasen T (2013) Preventing
cryptosporidiosis: the need for safe drinking water. Bull World Health
Organ 91: 238.
Volume 7 • Issue 1 • 1000261
Citation:
Samuel F (2016) Opportunistic Parasitism: Parasitic Association with the Host that has Compromised Immune System. J Bacteriol
Parasitol 7: 261. doi:10.4172/2155-9597.1000261
Page 4 of 4
24.
25.
26.
27.
28.
29.
30.
Marcos LA, Gotuzzo E (2013) Intestinal protozoan infections in the
immunocompromised host. Curr Opin Infect Dis 26: 295-301.
Zhou P, Chen Z, Li HL, Zheng H, He S, et al. (2011) Toxoplasma gondii
infection in humans in China. Parasit Vectors 4: 165.
Dubey JP, Tiao N, Gebreyes WA, Jones JL (2012) A Review of
Toxoplasmosis in Humans and Animals in Ethiopia. Epidemiol Infect
140: 1935-1938.
Halonen SK (2004) Immune Response to Toxoplasma Gondii in the
Central Nervous System. World Class Parasites 9: 67-88.
Sandhu A, Samra AK (2013) Opportunistic infections and disease
implications in HIV/AIDS. International Journal of Pharmaceutical
Science Invention 2: 47-54.
Ahmadpour E, Daryani A, Sharif M, Sarvi S, Aarabi M, et al. (2014)
Toxoplasmosis in immunocompromised patients in Iran: a systematic
review and meta-analysis. J Infect Dev Ctries. 8: 1503-1510.
Kim KH, Song KH, Jeon JH, Park WB, Park SW, et al. (2010) A Case of
Cerebral Toxoplasmosis Following Tandem Autologous Stem Cell
J Bacteriol Parasitol
ISSN:2155-9597 JBP, an open access journal
31.
32.
33.
34.
35.
Transplantation in a Multiple Myeloma Patient. Infect Chemother 42:
181-186.
Ardiç N (2009) An overview of Strongyloides stercoralis and its
infections. Mikrobiyol Bul 43: 169-177.
Schar F, Trostdorf U, Giardina F, Khieu V, Muth S, et al. (2013)
Strongyloides stercoralis: Global Distribution and Risk Factors. PLoS
Negl Trop Dis 7: e2288.
Keiser PB, Nutman TB (2004) Strongyloides stercoralis in the
Immunocompromised Population. Clin Microbiol Rev 17: 208-217.
Roxby AC, Gottlieb GS, Limaye AP (2009) Strongyloidiasis in transplant
patients. Clin Infect Dis 49: 1411-1423.
Lam CS, Tong MK, Chan KM, Siu YP (2006) Disseminated
strongyloidiasis: a retrospective study of clinical course and outcome. Eur
J Clin Microbiol Infect Dis 25: 14-18.
Volume 7 • Issue 1 • 1000261
Download